In diseases associated with chronic left ventricular (LV) hypertrophy, slowing of myocardial relaxation has been a characteristic finding; the mechanisms responsible for this abnormality are unknown. This study will test the hypothesis that slowing of myocardial relaxation in pressure-overload left ventricular hypertrophy is related in part to afterload mismatch (inappropriately high systolic wall stress) in the setting of potential myocardial ischemia. Normal subjects and patients with aortic stenosis in the absence of coronary artery disease will be studied using simultaneous micromanometer left ventricular pressure recordings and measurement of LV dimensions and wall thickness (ultrasound). The hypothesis will be tested by addressing 5 specific questions: (1) Is there a relationship between systolic wall stress and the peak rate of LV wall thinning (load-relaxation relationship) in normal subjects during the resting state and during pharmacologically imposed increases in load? I expect to find an inverse relationship between systolic LV wall stress and the peak rate of diastolic wall thinning; that is, the greater the load, the slower the relaxation rate. (2) Is there a comparable inverse load-relaxation relationship in patients with pressure-overload hypertrophy due to aortic stenosis, assessed in the resting state and during infusion of nitroprusside to decrease load? The hypothesis to be tested is that reduction of systolic wall stress in patients with aortic stenosis will be accompanied by restoration of myocardial relaxation towards normal. (3) What is the effect of transient ischemia induced by pacing tachycardia on the load-relaxation relationship in patients with pressure-overload hypertrophy? (4) What is the relationship between myocardial relaxation in patients with pressure-overload hypertrophy and the extent of hypertrophy per se? (5) What is the relationship between myocardial relaxation and myocardial fiber stiffness (radial stress-strain analysis) in normal subjects and in patients with pressure-overload hypertrophy? These studies will help to identify the determinants of myocardial relaxation in normal humans, and will clarify the contribution (if any) of high systolic wall stress to the slowing of myocardial relaxation characteristic of patients with chronic pressure-overload LV hypertrophy.